Cardiac arrest and cardiopulmonary resuscitation (CPR) are followed by coma and early death in up to 50% of cases, and in permanent brain damage in 20-40% of survivors. The Brain Resuscitation Clinical Trial (BRCT) I (1979-83) is an ongoing effective study mechanism, being used to evaluate the brain damage ameliorating effect of thiopental. Our preliminary data and recent animal data suggest that more effective therapy than barbiturates is needed. Recent experimental evidence suggest that calcium entry blockers can prevent or ameliorate postischemic cerebral hypoperfusion and long-term brain damage in animals. The proposed BRCT II (1983-86) will use the same clinical study mechanism as the BRCT I to collect data on at least 400 cases of cardiac arrest in over 10 hospitals. Goals of the study are: (1) to determine the ability of a calcium entry blocker given immediately postischemia to ameliorate brain damage; (2) to identify complications of the therapy; and (3) to study neurologic function and overall outcome during the 6 mos follow-up. Most patients will have pre-hospital sudden cardiac deaths. Patients will be entered immediately after restoration of adequate perfusion pressure if they are comatose. They will be assigned at random to blinded i.v. administration of the calcium entry blocker of choice or placebo, started at 0-30 min post-arrest and continued for 72 h postischemis. Both treatment groups will receive the same standard life support. Using methods of data collection, management and analysis adapted from the BRCT I, we will compare mortality, morbidity, neurologic disability and quality of life over 6 mos between control and treatment groups. Cerebral and overall performance categories (CPC, OPC) 1 (normal) and 2 (moderate disability) vs. 3 (severe disability), 4 (vegetative state), and 5 (brain death) will be the principal outcome measurements. Risks, benefits, balance of variables between groups, and adherance to to protocol will be monitored continuously. Data will also be analyzed to obtain epidemiologic information; to search for early PI changes predictive of outcome; to examine the effect of arrest time, CPR and post-CPR factors on outcome; to identify cerebral vs. noncerebral causes of mortality; and to evaluate long-term neuropsychological function and recovery.